4 tricks to increase the “good” cholesterol
September 20, 2008
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Stop smoking. This is an evidence !!
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Healthy Eating. Especially avoid Trans fats that foul the body by increasing the bad cholesterol.
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Sports. No need to exercise violently. 30 minutes 5 times a week is sufficient to increase good cholesterol by 5 to 10%.
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Lose weight. Lost 10 kilograms increase good cholesterol 1mg/dl.
Sophrology? What’s ?
September 20, 2008
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In medical practice of course.
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In the training and competition of every sports.
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In the Prevention and Control of Stress and personal development as human beings living in society today because of the mass disease that attacks the human values which constitute the immune system of society, in the same way that AIDS attacks the immune system of humans.
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In personal development as strengthening and activation of positive structures of the human being.
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The vivantiel training of healthy people to enhance their capabilities and existential values .
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As vivantiel training since childhood to death, reinforcing the different stages of life.
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For managers and employees in different companies, factories, banks and industries.
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For capacity building to be such as memory, concentration, etc.
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For gerontological and memory training groups.
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In tobacco control and anti-drug control.
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In training groups of the army and high-risk groups.
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As individual or groups in collaboration with organizations of prevention own social major cities
In large communities of the Third World, …
Type-2 Young Diabetic Men Suffer Low Testosterone Levels Which Affects Fertility, Muscle Mass, Heart Health
September 7, 2008
Young men with type 2 diabetes have significantly low levels of testosterone, endocrinologists at the University at Buffalo have found – a condition that could have a critical effect on their quality of life and on their ability to father children.
This study follows research published earlier by these scientists reporting that one-third of middle-aged men with type 2 diabetes have low testosterone levels, requiring treatment for erectile dysfunction.
“These new findings have several clinical implications besides the impairment of sexual function in these young men,” said Paresh Dandona, Ph.D., UB Distinguished Professor in the Department of Medicine and senior author on both studies.
“The lack of testosterone during these critical years may lead to diminished bone mass and the lack of development or loss of skeletal muscle. In addition, these patients may gain more weight (with an average body mass index of 38 they already were obese) and become more insulin resistant.
“Also, patients with low testosterone and type 2 diabetes have been shown to have very high concentrations of C reactive protein,” he added, “which increases their risk of developing atherosclerosis and heart disease above and beyond the risk associated with diabetes.”
Results of the new study appear in the online edition of Diabetes Care and will be published in an upcoming edition of the journal.
Anil Chandel, M.D., UB clinical assistant instructor and medical resident working with Dandona, is first author.
The current study was conducted in 38 men with type 1 diabetes and 24 men with type 2 diabetes who were referred to the Diabetes-Endocrinology Clinic of Western New York at Millard Fillmore Hospital of Kaleida Health, where Dandona is chief of the Division of Endocrinology.
The average age of men in the type 1 and type 2 groups was 26 and 27, respectively, with a range of 18-35 years.
Results showed that type 2 diabetics had half the amount of total and free testosterone in their blood as their type 1 counterparts. Free testosterone is the amount of the hormone not bound by protein molecules that can affect bodily functions.
Using the amount of free testosterone considered normal in men in general, eight out of the 24 type 2 diabetics had below-normal concentrations. However, using the normal range for men of their age, 14 out of the 24, or 58 percent of the young type 2 diabetics had lower than normal testosterone levels. Type 1 diabetics, meanwhile, had normal levels of total and free testosterone for their age group.
Patients with below-normal testosterone also had low levels of luteinizing hormone (LH) and follicle-stimulating hormone (FSH), which are released by the pituitary gland and are essential for testosterone secretion and normal fertility. Low levels of all three hormones results in a syndrome known as hypogonadotropic hypogonadism.
“While obesity contributes to the association of type 2 diabetes and hypogonadotropic hypogonadism (HH), the association is not dependent entirely on obesity,” said Dandona. “In our first study of diabetic men, we found that 31 percent of lean type 2 diabetics also had HH, so it is likely that factors other than obesity contribute to HH, possibly insulin resistance. Type 2 diabetic patients generally have higher insulin resistance, while all obese men are not insulin resistant.
“Whether obesity or insulin resistance is the major determinant of HH has to be addressed in future studies, and the pathogenesis of HH needs to be defined,” he said. Dandona’s group currently is investigating these questions.
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Article adapted by Medical News Today from original press release.
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So, and???
A good reason to seek the deficit in testosterone and fix it. And not only among diabetics of course.
Coronary artery disease, don’t forget the sub-clinical hypothyroidism
September 6, 2008
A meta-analysis provides a negative impact on the sub-clinical hypothyroidism on cardiovascular risk factors. (This confirmme my practice and those of any anti aging physicianan) indeed, it increases significantly the risk of coronary disease, with an odds ratio, which reached 1.65 overall. If the analysis is limited to 9 studies with adjusting for demographics, Odds Ratio previous rises to 1.81. It reached 2.38 when the studies are included with adjusting for cardiovascular risk factors.
The analysis by subgroups based on the type of study gives somewhat different results. GOLD east of 1.42 in the prospective cohort studies and 1.72 in case-control studies or studies cross.
This meta-analysis appears to confirm the adverse impact of hypothyroidism infra clinic on the risk of coronary disease. It remains to demonstrate that the hormone is able to reverse this trend.
PROGESTERONE FOR THE BRAIN
September 6, 2008
The progesterone could be use in brain trauma treatment?
A first study in humans seems to confirm this hypothesis already observed in animals, in which the progesterone helps reduce intracranial pressure.
On hundred people had visited the hospital in the eleven hours after a head injury moderate or severe, 77 received progesterone in IV and 23 a placebo IV. Among those severely affected, 40% of those on placebo died within thirty days against 13% in the progesterone group.
However, no difference in deaths was found among those moderately affected.
Subclinical Hypothyroidism: not so benign…
September 6, 2008
This is by definition hypothyroïdies for which the value of TSH is increased while the rate of free T4 remains normal (and, if the measured-which is usually not the case in France – The T3). The value adopted for TSH is 4 mIU / l in the French recommendations. But this threshold has been discussed, and American teams have proposed to lower to 2.5 mIU / l.
That’s a good news and i hope many french physicians will do as our american friends. But i note that Antiagning physicians use it for a long time.
Insulin Found To Play Previously Unknown Role In Aging And Lifespan
September 5, 2008
Researchers at the Joslin Diabetes Center have shown that insulin has a previously unknown effect that plays a role in aging and lifespan, a finding that could ultimately provide a mechanism for gene manipulations that could help people live longer and healthier lives.The paper, published in the March 21st issue of Cell, reports that insulin inhibits a master gene regulator protein known as SKN-1, and that increased SKN-1 activity increases lifespan. SKN-1 controls what is called the Phase 2 detoxification pathway, a network of genes that defends cells and tissue against oxidative stress – damage caused by elevated levels of free radicals (byproducts of metabolism) – and various environmental toxins. The new finding was demonstrated in experiments on the digestive system of C. elegans, a microscopic worm often used as a model organism.
“We’ve found something new that insulin does and it has to be considered when we think about how insulin is affecting our cells and bodies,” said Dr. T. Keith Blackwell, senior investigator at Joslin and author of the paper. “This has implications for basic biology since under some circumstances insulin may reduce defense against the damaging effects of oxidative stress more than we realize.”
The idea down the line is that fine-tuning the activity of SKN-1 may lead to increased resistance to chronic diseases and influence longevity, he said. The work could be important as it relates to diabetes and the many problems associated with the disease, particularly vascular and renal complications.
But, today’s finding may be most important for what it teaches about aging in general, he said.
“The major implication is that we have found something new that affects lifespan and aging, and an important new effect that insulin and/or a related hormone called insulin-like growth factor-1 may have in some tissues,” said Blackwell. “The implications go far beyond diabetes.”
It has been known since the 1990s that insulin inhibits a gene regulator protein known as FOXO, important in diabetes metabolism, tumor suppression and stem cell maintenance. FOXO controls a number of genes, including many involved in stress resistance. Studies in C. elegans showed that reduced insulin signaling boosted activity of a FOXO protein known as DAF-16, leading to greater stress resistance and longer life.
The new work places SKN-1 alongside FOXO as a second master gene regulator that is inhibited by insulin signaling and adds to the body of knowledge about insulin and its effects on gene pathways, stress resistance and aging. According to the paper, insulin’s effect on SKN-1 occurs independently of its effect on DAF-16.
“You can manipulate the expression of SKN-1 and the worms live longer,” said Blackwell, an Associate Professor of Pathology at Harvard Medical School and faculty member at the Harvard Stem Cell Institute.
The experiments will have to be repeated in mammals, where insulin and insulin-like growth factor-1 have a complex array of effects in different tissues. But, according to Blackwell, other findings in the C. elegans model have generally turned out to be applicable to mice and humans.
Blackwell’s lab at Joslin is focusing on mechanisms of free radical resistance and aging, and on gene regulation mechanisms in C. elegans stem cells with the idea of using this knowledge towards reprogramming human stem cells into insulin-producing cells.
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Article adapted by Medical News Today from original press release.
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The research was funded by the National Institutes of Health and The Iacocca Foundation, the Fonds der Chemischen Industrie, BMBF NGFN2, Qualitaetsoffensive BW and Deutsche Forschungsgemeinschaft CRC746 and EC Network of Excellence Lifespan, as well as an NRSA, an NIH training grant, KRF and MOST/KOSEF.
Other researchers involved in the paper were Jennifer M.A. Tullet, Joseph Baker and Riva P. Oliveira of Joslin; Jae Hyung An of Joslin and Yonsei University in Korea; Ji Yun Hwang of Yonsei University; and Shi Liu, Ralf Baumeister and Maren Hertweck of the University of Freiburg.
About Joslin Diabetes Center
Joslin Diabetes Center is the world’s largest diabetes clinic, diabetes research center and provider of diabetes education. Joslin is dedicated to ensuring people with diabetes live long, healthy lives and offers real hope and progress toward diabetes prevention and a cure for the disease. Founded in 1898 by Elliott P. Joslin, M.D., Joslin is an independent nonprofit institution affiliated with Harvard Medical School. For more information on Joslin, visit
http://www.joslin.org/.Source: Kira Jastive